Patients suffering ulcer-like or hyperacidity symptoms may be treated by established anti-ulcer drugs like Tagamet.RTM. (cimetidine) or Zantac.RTM. (ranitidine hydrochloride), which slow down the rate of acid secretion by the stomach. Patients maintained on the standard anti-ulcer drug regimen for one week generally exhibit a fairly rapid and favorable response, but unless continuously administered, patients soon suffer recurrences of their symptoms. Patients may also be treated with liquid or tablet antacid agents which coat the lining of the stomach and/or reduce acidity. These regimens are merely palliative. In advanced cases, surgery may be required.
For some time now, it has been speculated that the bacterium Helicobacter pylori plays an etiologic role in the development of both duodenal and gastric ulcers, and in chronic gastritis. Specifically, some Australian researchers have hypothesized that the Helicobacter pylori microorganism lives and grows between the inner lining of the stomach and under the protective mucous coat which protects the stomach lining from the corrosive effects of stomach acid. See Lancet. 1983; Vol. 1, pages 1273-5; Lancet. 1984; Vol. 1, pages 1311-5.
Bacteria in the stomach are typically killed by acid secreted by the cells lining the stomach. Similarly, with Helicobacter pylori, the stomach lining senses that the Helicobacter pylori bacteria are present and causing infection. In response, the stomach lining cells increase their production of stomach acid to try and kill the Helicobacter pylori bacteria. The area between the mucous coat and the stomach inner lining inhabited by the Helicobacter pylori is, however, a difficult area for the acids to penetrate because of the overlying protective stomach mucous coating.
Consequently, the acid produced in response to the bacteria flows downstream from the stomach and may cause gastric or duodenal ulcers. It is also possible that areas of the stomach directly infected by the Helicobacter pylori bacteria also develop ulcerations.
Research studies have established a link between the presence of chronic antral gastritis, and gastric and duodenal ulcers, and Helicobacter pylori gastric infection. Seventy to eighty-five percent of biopsy specimens from patients with chronic gastritis test positive for this organism.
Attempts to treat the organism with known regimens have proved ineffective, however. In 1985, Langenberg et al. reported attempts to eliminate the Helicobacter pylori organism from the inner stomach lining. Administration of bismuth to infected patients was found to result in diminution of symptoms, and endoscopic examinations did not detect the presence of Helicobacter pylori organisms in eleven of eighteen patients maintained on bismuth for up to eight weeks. The antibiotic amoxicillin was found to reduce the number of Helicobacter gastric organisms in seven of eight patients treated for four weeks. However, three each of the bismuth and amoxicillin treated patients were found to have Helicobacter pylori organisms on the inner stomach lining after being studied four to thirteen weeks following completion of their therapies. Subsequent bacterial infection with another strain of Helicobacter pylori was eliminated as a possibility. Langenberg, Rauws, et al. The pathogenic role of Campylobacter pylori studies by attempts to eliminate these organisms. Abstract 98 in Proceedings of the Third International Workshop on Campylobacter Infections. Pearson et al, eds. Public Health Laboratory Service. 1985; 165-66.
Experiments with other antibiotics, such as tinidazole and doxycycline in conjunction with bismuth were similarly ineffective.
In fact, studies have shown that a majority of patients who showed negative endoscopic cultures for Helicobacter pylori at the completion of standard antibiotic treatments were found to have positive Helicobacter pylori cultures within four weeks after finishing treatment. Thus, it appears that these patients had their Helicobacter pylori infections suppressed by the treatments without eradication of the offending organism. While various anti-bacterial regimens are more successful in treating chronic gastritis and gastric and duodenal ulcers than palliative regimens only, the known antibacterial treatments used in the various studies have thus far failed to result in reliable high rates of eradication of Helicobacter pylori lasting more than four weeks.
The failure of antibiotics thus far to reliably eradicate the Helicobacter pylori organism may be due to the inability of most orally administered antibiotics to adequately penetrate the space between the inner stomach lining and the stomach protective mucous layer. This failure would explain the antibiotic suppression, but not eradication, of Helicobacter pylori organisms.
In fact, investigators have noted that the use of common antibiotics to treat gastric Helicobacter pylori infections is associated with an eventual almost one hundred percent relapse rate. Czinn and Speck. Campylobacter pylori: a new pathogen. J. Peds. 1989; 144:670-672.
Thus, as with known regimens, the antibiotic and chemical treatments are merely palliative. It would be desirable then to find an antibiotic which is able to penetrate the space under the gastric mucous layer in an amount effective to produce more successful treatment of Helicobacter pylori infections.